sick sinus syndrome 1

8/16/2019 Sick Sinus Syndrome 1

1/23

PATIENT PROFILE

Name of patient : Mr.Jalesh

Age : 35 yrs

Address : C/o saradha

Panickal Hose

Alapp!ha

Marital stats : married

"ccpation : coolie

#ate of Admission : $/5/%&'(

) P Nm*er : &'%5+$

,ard and nit : -ard'%

Chief complaints on : sdden -eakness -ith syncope

#iagnosis : ick ins syndrome

PRESENT MEDICAL HISTORY

Mr.Jalesh -as apparently normal till $/5/%&'( after that he got admitted in the general hospital

follo-ed *y -eakness and syncope from there C0 -as taken it -as sho-n a*normality in the

rhythm and patient -as transferred to 1#MCH 2andanam on Admission the 4ital signs -as

plse 3% */mt 6P'3&/7&respiration%$ and C0 -as repeated -hich sho-ed ick sins

syndrome and patient got admitted in -ard '%. No- he is on *eta adrenergic agonist and nder

o*ser4ation


2/23

PAST MEDICAL HISTORY

Patient has no significant past history of diseases like hypertension and dia*etes. History of

septal defect in the childhood . 8ele4ant medical data not a4aila*le

FAMILY HISTORY

1here is no history of any heart disease or other congenital disorders in the family

Family Tree

aradha Jalesh

PERSONAL HISTORY

• #iet pattern : Non4egetarian lack of appetite in recent period

•

6o-el and *ladder ha*its : Normal and irreglar *o-el and *ladder ha*its• leeping ha*its :8eglar *t no- decreased sleep de to pleritic chest pain cogh 9

mild hemoptysis

• nhealthy ha*its : History of alcoholism and smoking

SOCIO-ECONMICAL HISTORY

Patient comes from a middle class family.he is married and has ' childrenshe maintains good

interpersonal relationship -ith family mem*ers and neigh*ors. He is the *read-inner of the

hose.

PHYSICAL ASSESSMENT (DONE ON 4/5/20!"


3/23

# $e%eral A&&eara%'e

Height : '($cm

,eight : 5% kg

0eneral hygiene : satisfactory

6ody *ilt : Moderately *ilt

2# i)al Si*%+

1emperatre : +7.(;<

Plse rate : $&/min

8espiration rate : %7/*reath/min

6lood Pressre : '3&/ =& mmHg

,# Hea ). ..) eami%a)i.%

Hea Normal in shape no a*normalities *lack hair

Fa'e ymmetrical facial featres no facial pffiness.

Eye+ Ppils e>al and reacting to light P&&&8 &?&A&

N.+e no de4iation in nasal septm nasal flaring a*sent 1

M.)3 oral mcosa is pink tonge in midline

Ne' No tracheal shift cer4ical lymph node enlargement present

C3e+) Air entry is *ilaterally e>al and 6ilateral

8espiratory rate @ %7/minte

)nspection: 6ilaterally epanding chest no enlarged tmors

Palpation: No enlarged lymph nodesdecreased tactile fremits.


4/23

Percssion: )ncreased diaphragmatic ecrsion

Ascltation: *ronchial and *roncho4esiclar sond apical plse $&*/mt

A.me% oft no distention or tenderness

)nspection: no distensionsymmetrical in appearance

Ascltation: decreased *o-el sondsno *or*orgomi

Palpation: no tenderness hepatosplenomegaly HM

Percssion: no flid/thrill

$e%i)alia- no a*normalities or discharge in genital area no ind-elling catheter present

E)remi)ie+ No *ilateral pitting edema present cold etremities mo4ing all for lim* t-o

cannla present on left hand

4# Sy+)em 6i+e eami%a)i.%

Ce%)ral Ner7.+ Eami%a)i.%

Patient is conscios0C cale B $25M(

Higher mental fnction Client is consciosoriented to time place and person

ensory fnction B intact

8eflees B intact

Cari.-7a+'lar +y+)em

Plse rate B $&/min reglar

6lood pressre B '3&/=& mmHg

Capillary refill B -ithin % seconds

Heart sonds B ' % heard

Peripheral plses B palpa*le

tremities B coldno edema


5/23

J2P B not ele4ated

Re+&ira).ry +y+)em

)nspection B 8espiratory rate is %7/*reath/min

Palpation: No enlarged lymph nodes normal tactile fremits.

Percssion: normal diaphragmatic ecrsion

Ascltation: no ad4entitios *reath sonds

$a+)r.-i%)e+)i%al +y+)em

"ral mcosa B moist

6o-el sonds norml *o-el sonds

M+'l.-+ele)al +y+)em

Mo4ing all for lim*s

I%)e*me%)ary +y+)em

kin B moist

dema B not present

$e%i).-ri%ary +y+)em

No a*normal discharges no fol smell


6/23

Si%+ N.e Dy+%')i.%(sick sinus syndrome)

ins node dysfnction is a common clinical syndrome comprising a -ide range of

electrophysiologic a*normalities from failre of implse generation failre of implse

transmission to the atria inade>ate s*sidiary pacemaker acti4ity and increased sscepti*ility

to atrial tachyarrhythmias.$ 1his disorder has also *een 4aria*ly termed the sick sinus

syndrome,tachycardia-bradycardia syndrome,SA disease, and SA dysfunction.

E)i.l.*y . Si%+ N.e Dy+%')i.%

Althogh the eact etiology of N# is sally not identified most cases are *elie4ed to *eattri*ta*le to a com*ination of 4arios i%)ri%+i' processes that directly affect the anatomy and

physiology of the sins node and/or the srronding atrial tisseD and e)ri%+i' factors

processes that affect sins node fnction in the a*sence of strctral a*normalitiesD. 1he mostcommon intrinsic cases are cardiac agerelated N changes and coronary artery disease. 1he

most common etrinsic cases are medications and atonomic hyperacti4ity.

1)"?"0)C


7/23

I%)ri%+i' SND

Age-related changes

Agerelated changes are *elie4ed to *e the most common case of N# and are related tofi*rosis in the N. 1hese fi*rotic changes also occr in the atrim and the condction system of

the heart and are *elie4ed to contri*te to the association among N# tachy*rady syndromecondcti4e system disease and an inappropriately slo- escape rhythm.

1he pacemaker acti4ity in the N has *een fond to *e related to 4oltage and calcim

clocks. Agerelated do-nreglation of calcim channel epression in the N has *een sggestedas a potential case of N# -ith aging.

Coronary artery disease

Coronary artery disease is *elie4ed to *e a common contri*tory case of N# pro*a*ly

throgh atherosclerotic changes in the N artery.

Genetic causes

N# may *e familial an atosomal dominant pattern of inheritance has *een descri*ed.

e4eral moleclar defects in hman hearts defects in the sodim channel calcim channelhyperpolari!ationacti4ated cyclic ncleotidegated cation HCND channel ankyrin6 and

connein ha4e *een associated -ith familial sick sins syndromes.

)n addition N# is seen in children -ith congenital and ac>ired heart disease particlarly after

correcti4e srgery. 1he case of N# in these children is likely related to the nderlying

strctral heart disease and srgical trama to the N and/or N artery..

)n addition sins 4enoss atrial septal defect A#D *stein anomaly and heterotaysyndromes particlarly left atrial isomerism can lead to N#.

Mechanisms in tachy-brady syndrome

1achycardiamediated remodeling of the N is present in patients -ith atrial

fi*rillation/fltter and it may contri*te to N# in these patients. )n patients -ith tachy*rady

syndrome atrial fi*rillation a*lation can re4erse N# as e4idenced *y a redction in Nreco4ery time an increase in mean and maimal heart rates and a lack of symptoms related to

sins *radycardia or pase. 1he mechanism of N# in tachy*rady syndrome may in4ol4e the

a*normal fnction of 4oltage and calcim clocks in the N.

Other heart diseases

"ther strctral heart diseases are ncommon cases of N#. 1hese inclde *t are not limited

to the follo-ing:

• 2arios cardiomyopathies

• Myocarditis

• Pericarditis

http://emedicine.medscape.com/article/892151-overviewhttp://emedicine.medscape.com/article/892151-overviewhttp://emedicine.medscape.com/article/889613-overviewhttp://emedicine.medscape.com/article/892151-overviewhttp://emedicine.medscape.com/article/889613-overview


8/23

• )nfiltrati4e heart diseases Amyloidosis hemochromatosis neoplasm

• Collagen 4asclar diseases ystemic lps scleroderma

• Neromsclar diseases Myotonic dystrophy


9/23

• N# may occr after repair of partial anomalos plmonary 4enos retrn

PAP28D or total anomalos plmonary 4enos retrn 1AP28D

• Cannlation of the sperior 4ena ca4a 2CD sally performed for cardioplmonary

*ypass or etracorporeal mem*rane oygenation CM"D may damage N tisse.

• )schemic cardiac arrest may case N#.

O)3er

8hematic fe4er is another case of N#. ch dysfnction may also reslt from CN

disease -hich is sally secondary to increased intracranial pressre -ith s*se>ent increase in

the parasympathetic tone.

ndocrinemeta*olic diseases hypothyroidism and hypothermiaD and electrolyte im*alances

hypokalemia and hypocalcemiaD are other conditions that can contri*te to N#.

A stdy *y naga et al of %&% s*Fects indicated that in patients -ith persistent atrialfi*rillation those -ith lo-amplitde fi*rillatory -a4es and a large left atrial 4olme inde are at

increased risk for the appearance of concealed N# after catheter a*lation has restored sinsrhythm.

F.r my &a)ie%) +e&)al a%.rmali)y 6a+ &re+e%) ) 3e 6a+ %.) %er*.%e a%y '.rre')i7e

+r*ery.

PATHOPHYSIOLO$Y

E)i.l.*i'al a').r+

De*e%era)i7e '3a%*e+ i% )3e S#A %.e

N.rmal 'ell+ i% )3e S#A %.e i+ re&la'e y ir..+ )i++e

A%.rmal im&l+e *e%era)i.% r.m S#A %.e( i%'rea+e .r

e'rea+e"

http://emedicine.medscape.com/article/897686-overviewhttp://emedicine.medscape.com/article/897686-overviewhttp://emedicine.medscape.com/article/899491-overviewhttp://emedicine.medscape.com/article/897686-overviewhttp://emedicine.medscape.com/article/897686-overviewhttp://emedicine.medscape.com/article/899491-overview


10/23

I%ae9a)e :LOOD S;PPLY TO ARIO;S PARTS OF THE

:ODY


11/23

pecific symptoms of N# inclde the follo-ing:

• Cere*ral symptoms )rrita*ility la*ile mood s-ings forgetflness di!!iness slrred

speech *lanking periods falls and syncope

• Cardiac symptoms Palpitations angina CH< symptoms and sdden cardiac death

rareD• 2age gastrointestinal symptoms and oligria

• Patients -ith tachy*rady syndrome may ha4e symptoms of stroke or transient ischemia

attack 1)AD

• ercise intolerance

•


12/23

screening is typically reser4ed for patients in -hom specific clinical factors sggest the

diagnosis.

E'3.'ari.*ra&3y

No specific imaging stdies are re>ired in the initial -orkp of N#. Ho-e4er an

echocardiogram shold *e considered *ecase it can docment the presence of nderlying4al4lar or ischemic heart disease and may sggest the diagnosis of amyloid -hen diffse

condction system findings are present.

)n addition this stdy is sita*le for the e4alation of 4entriclar fnction and is also sefl in patients -ith coeistent CH# for the assessment of associated anatomic and hemodynamic

a*normalities.

Tra%+e+.&3a*eal a)rial &a'i%*

sophageal P stdy constittes a relati4ely safe and inepensi4e method to detect N# *ydetermining N reco4ery time in patients -ho present -ith di!!iness or syncope and

palpitations.

lectrocardiography

lectrocardiographic criteria for N# inclde the presence of ' or more of the follo-ing see theimages *elo-D:

• ins *radycardia *elo- the heart rate epected for age )e nder '&& *eats per minte

*pmD in an infant nder 7& *pm in a preschool child nder (& *pm in a school child and

nder 5& *pm in an adolescent

• ins pase or a*sence of an epected P -a4e for more than 3 seconds May *e de to

sins arrest failre of the N pacemaker cells to depolari!eD or *e the reslt of sinoatrial eit

*lock depolari!ation of the N *t failre to condct to the atriaD

• lo- escape rhythms that originate -ithin the atria His *ndle or 4entricles

• Marked sins arrhythmia -ith constant 4ariation in the PP inter4al -hich is likely to *e

accompanied *y sins *radycardia

• Presence of *oth *radyarrhythmias and tachyarrhythmias )e N reentry tachycardia

atrial tachycardias from an ectopic focs atrial fltter and atrial fi*rillation

I%a&&r.&ria)e +i%+ ray'aria

1he ar*itrary ctoff for a lo- sins rate in a person -ho is at rest *t a-ake is sally defined as

nder 55(& *pm. Ho-e4er a stdy in 5&& healthy s*Fects sggested that the lo- afternoon

sins rate for men and -omen shold *e arond $( and 5' *pm respecti4ely. Pacemaker therapy

is a class ))* indication for patients -ith minimal symptoms and a chronic heart rate of less than

$& *pm -hile a-ake according to the %&&7 gidelines from the American College of CardiologyACCD/American Heart Association AHAD/Heart 8hythm ociety H8D. A focsed pdate of

these gidelines -as p*lished in %&'3.

Si%+ &a+e .r arre+)

ins pase or arrest is defined as a*sence of sins P -a4es on the electrocardiogram C0D for

more than % seconds de to a lack of sins nodal pacemaker acti4ity. 1he dration of the pases

shold ha4e no arithmetical relationship to the *aseline sins rate ie the PP inter4al shold not

http://emedicine.medscape.com/article/894226-overviewhttp://emedicine.medscape.com/article/894226-overviewhttp://emedicine.medscape.com/article/894226-overview


13/23

*e an inter4al of the paseDK other-ise the diagnosis of sinoatrial eit *lock shold *e

considered. ymptomatic long sins pases or arrests in patients -ith N# often occr after the

termination of atrial fi*rillation or atrial fltter.

A sins pase of % seconds is not nsal in a healthy person. Ho-e4er a sins pase of morethan 3 seconds is 4ery ncommon ecept nder certain conditions sch as sleep apnea

hyper4agotonia state or sei!re acti4ity

Si%.a)rial ei) l.'

First degree


14/23

An escape rhythm may also originate *elo- the atria at the HisPrkinFe Fnction ie Fnctional

escape rhythm -ith a rate of (&7& min in infants and 5&=& min in childrenD or lo-er if

originating in the 4entricles ie 4entriclar escape rhythmD. 1he frther *elo- the atria theescape rhythm originates the slo-er the rate.

scape rhythms -hich are those that occr *y defalt shold *e distingished from srpation

rhythms -hich are those that occr *ecase of increased atomaticity from pacemakers that fire

at a faster rate than the N.

C3r.%.)r.&i' i%'.m&e)e%'e

6ecase the N sally responds to atonomic ner4os system inpt eercise increases the heart

rate in response to increased sympathetic tone. Patients -ith N# sally ha4e a *lntedresponse. 1herefore an eercise stress test can determine -hether chronotropic incompetence is

present.

Chronotropic incompetence is defined as failre to achie4e =&7&G of maimal predicted heart

rate maimal predicted heart rate @ %%& ageD at peak eercise. 1he clinical 4ale of thisdefinition ho-e4er has not *een -ell 4alidated.L%5 1he peak eercise heart rate can *e

inflenced *y mltiple factors.

Ta'3y-ray +y%r.me

6radyarrhythmiastachyarrhythmias occr -hen *radycardia and tachycardia alternate. 1he

*radycardia may originate in the sins atria A2 Fnction or 4entricleK the tachycardia is sallycased *y atrial fltter or fi*rillation althogh it can also *e cased al*eit less commonly *y

reentrant spra4entriclar tachycardia in the N or atrial mscle.

Holter Monitoring

8ecording the C0 for %$$7 hors is sefl in the assessment of N# related to the pre4ioslyeplained C0 findings that may *e present.

1he specificity of a direct o*ser4ation of spontaneos ie not pro4oked *y P stdyD N# is'&&G and an P stdy is not re>ired. 1herefore cardiac monitoring rather than P stdy is the

method of choice to assess N#.

A %$hor Holter stdy also has the ad4antage of re4ealing -hether N# prodces symptoms

sch as di!!iness presyncope or syncopeK these cannot *e determined dring an P stdy *ecase the patient is hea4ily sedated. 1herefore a %$hor Holter stdy can help decide if

pacemaker therapy is re>ired.

Pharmacologic timlation 1ests

#e to their moderate sensiti4ity and specificity for N# diagnosis intrinsic heart rate and

atropine stimlation tests are occasionally sed as accessory tests in selected patients sch asthose -ith sspected hyper4agotoniaD. 1he 4ale of isoproterenol propranolol and adenosine

stimlation tests in N# diagnosis is more contro4ersial.

I%)ri%+i' 3ear) ra)e

http://emedicine.medscape.com/article/1971142-overviewhttp://emedicine.medscape.com/article/1971142-overview


15/23

Atropine &.&$ mg/kgD and propranolol &.% mg/kgD ha4e *een sed to pharmacologically

dener4ate the N -hich is then follo-ed 5%& mintes later *y an e4alation of its intrinsic heart

rate )H8D. 1he )H8 in a healthy person is approimately e>al to ''=.% B &.53 AgeD.

)ntrinsic N# is presmed to *e present if the sins rate after medications is *elo- the calclated)H8. Patients -ith mild N# may ha4e a normal or eacer*ated response. 1his test is pro*a*ly

helpfl in patients -ith sins *radycardia de to sspected hyper4agotonia L%( in -hom the )H8

is epected to *e normal.

A)r.&i%e )e+)

Atropine alone p to &.&$ mg/kgD may pro4ide as mch information as the com*ination of

atropine &.&$ mg/kgD and propranolol &.% mg/kgD. L%= Atropine '3 mgD is the most commonly

sed agent to assess the parasympathetic tone. A normal response is an increase in the sins ratea*o4e +& *pm or an increase of more than %5G a*o4e the *aseline sins rate. L%5 Patients -ith

symptomatic N# sally demonstrate a decrease in )H8. Ho-e4er patients -ith only mild

N# may ha4e a normal or eacer*ated response to atropine

lectrophysiologic tdiesP stdies are indicated in patients -ith signs of *radyarrhythmias mainly syncopeD in -hom

*radycardia cold not *e docmented dring Holter monitoring. Classic P criteria for N#

inclde the presence of ' or more of the follo-ing:

• Corrected N reco4ery time CN81D greater than %=5 milliseconds

• A condction time greater than %&& milliseconds

• A node arrest

• A eit *lock

• N reentry tachycardia

SN re'.7ery )imeP stdies can docment N# -hen stdying N atomaticity *y directly recording electricalacti4ity. "ne P catheter -hich has % proimal electrodes that record the H8A electrogram and

% distal electrodes to pace the H8A near the N is positioned in the 8A.

A second P catheter -hich is sed to record lo- 8A ?8AD electrical acti4ity is positioned

across the tricspid 4al4e.

Measrement of N81 is achie4ed *y pacing the atrim. Pacing shold *e performed in the

H8A near the N at the Fnction of the sperior 4ena ca4a 2CD and the 8A for $( trials of 3&seconds each. ach trial shold se sccessi4ely shorter pacing cycle lengths eg (&& ms 55&

ms 5&& msD *eginning -ith a cycle length Fst shorter than the resting sins cycle length. N81

is the time inter4al *et-een the last paced captred *eat to the first spontaneos sins *eat.

0radal retrn of the N to its *aseline rate occrs o4er 5( *eats. Prolonged pases iesecondary pasesD can occr after the initial reco4ery inter4al in N#.

)f the longest inter4al for the reco4ery inter4al or secondary pase eceeds '5&& ms the N81 is

prolonged.


16/23

1o adFst for heart rate and *efore each pacing increase the resting sins cycle length C?D is

measred. ,hen the resting C? is s*tracted from N81 the CN81 is o*tained. )ts pper

reference range limit is 5%5 msK if the N81 eceeds the C? *y more than 5%5 ms the N81 isa*normal. 1he same occrs if the ratio of N81 to C? ie N81/C? '&&D is more than

'(&G.

Si%.a)rial '.%')i.% )ime

AC1 is another parameter to se in assessing N fnction. )t is the time inter4al in millisecondsfor an implse that originates in the N to condct throgh the perinodal tisse to the adFacent

right atrial tisse. 1he tisse that srronds the N or perinodal tisse has characteristics that are

similar to those of the A2 node.D

ight prematre atrial contractions PACsD are fired in the H8A at 5'& *pm faster than the Nrate *efore they are stopped a*rptly.

AC1 represents the time in milliseconds that it takes for the PAC fired in the H8A to enter and

reset the N. )t also represents the time for the ne- spontaneos N implse ie C?D to reach

the H8A. AC1 is measred as the time in milliseconds from the last PAC to the firstspontaneos sins *eat.

,hen the time inter4al *et-een the last spontaneos N depolari!ation ie *efore the PACD andthe one that occrred after a PAC is less than t-ice the 4ale of the % pre4ios spontaneos N

depolari!ations reset of the N *y the PAC has occrred.

AC1 can *e calclated as the inter4al from the PAC to the net spontaneos N *eat -hich

incldes condction throgh the perinodal tisse into the N resetting the N and condctionthrogh the same perinodal tisse *ack into the H8A ie Lretrn inter4al C?/%D. 1he

reference range is 5&'%5 ms in children and %&&%5& ms in adlts.

)f the N cannot prodce a spontaneos implse follo-ing PACs ie these ha4e not reset the Nand therefore AC1 cannot *e calclatedD A entrance *lock is present.

1his *lock cold *e cased *y markedly prolonged A condction and/or increased refractory period of periN or N fi*ers *oth of -hich indicate N#. N entrance *lock alternating -ith

reset responses also denotes N#.

N reentry tachycardia occrs -hen acti4ation of the atrim dring the spra4entriclar

tachycardia is the same as sins *eats ie P-a4e ais and morphology are the same as those in

the sins rhythmD. )t is sally indicati4e of N#.

C.m&li'a)i.%+

Complications from a diagnostic P stdy are rare *t may inclde the follo-ing:

• Hematoma at the pnctre site in the groin and or neck

• Hemorrhage

• )nfection cased *y maniplation of catheters inside the heart theoretical riskD

• Perforation pon catheter maniplation inside the heart of small patients most commonly

in4ol4ing the right atrial appendage and the right 4entriclar 82D otflo- tractD


17/23

1he complications of N# inclde the follo-ing:

• dden cardiac death rareD

• yncope

•


18/23

Die)

Patients -ith 4aso4agal syncope may re>ire increased dietary salt intake.

A')i7i)y

Patients -ith symptomatic N# -ho are not on pacemaker therapy shold titrate their le4el of

acti4ity to minimi!e symptoms.

C.%+l)a)i.%+

1hese inclde cardiac electrophysiology consltation.

Tra%+er

1ransfer patients for complicated dysrhythmias and pacemaker implant.

Pacemaker 1herapy

Pacemaker therapy is the only effecti4e srgical care for patients -ith chronic symptomatic

N#.

6ecase the incidence of sdden death in patients -ith N# is etremely lo- and pacemaker therapy does not appear to affect sr4i4al the maFor goal of pacemaker therapy in patients -ith

N# is to relie4e symptoms.

Pa'emaer i%i'a)i.%+

According to the %&&7 ACC/AHA/H8 gidelines pdated in %&'3D pacemaker therapy has thefollo-ing indicationsL% 3 :

• Class ) indication


19/23

1his practice is spported *y data from the #anish Mlticenter 8andomi!ed 1rial on ingle ?ead

Atrial Pacing 4erss #al Cham*er Pacing in ick ins yndrome #ANPACD trial in -hich

+.3G of patients -ith singlelead atrial pacing AA)8D re>ired pgrade to a dalcham*er pacemaker ###8D o4er 5.$ years follo-p de to ne- de4elopment of significant A2

condction a*normalities. 1his -as necessary despite the fact that these patients had no

significant intra4entriclar condction a*normality P8 inter4als *elo- %(&ms and no,encke*ach A2 *lock -ith atrial pacing at '&& *pm at *aseline.L3&

)n addition patients in AA)8 mode had more atrial fi*rillation than did patients in ###8 mode.

)mportantly ho-e4er no significant mortality difference *et-een AA)8 and ###8 mode -as

noted.

Arga*ly a singlecham*er atrial pacemaker -ith AA) mode is an accepta*le alternati4e in patients -ith N# and normal A2 and intra4entriclar condction *ecase of the added epense

of and the potential for more lead etraction -ith a dalcham*er pacemaker.

)n patients -ith N# and kno-n A2 condction a*normality inclding *ndle *ranch *lock and

*ifasciclar *lockD a dalcham*er pacemaker shold *e sed de to the high risk of A2 *lock a*ot 3(G in a 5year follo-p stdyD.

Pa'emaer &r.*rammi%* ea)re+

Chronic right 4entriclar pacing has *een sho-n to *e associated -ith an increased incidence of

atrial fi*rillation stroke heart failre and pro*a*ly death. L'7 3' 3% A stdy sggested that 82

pacing is detrimental to left 4entriclar ?2D fnction e4en in patients -ith a normal ?2 eFectionfraction ?2


20/23

8ate response featres ha4e *een sed in patients -ith N# especially in the presence of

chronotropic incompetence. Ho-e4er the clinical *enefits of this program featre are still

contro4ersial.L3(

?ong1erm Monitoring

Asymptomatic patients -ith N# shold *e o*ser4ed for symptoms. )n patients -ith a pacemaker carry ot the follo-ing on rotine pacemaker interrogations:

• Monitor leads and *attery stats

• nsre ade>ate heart rate spport at rest dring daily acti4ities and dring eercise

• Monitor for pacemaker malfnction sch as pacemakermediated tachycardia

• nsre minimal 82 pacing.

• Monitor for atrial fi*rillation and atrial fltter e4ents

Pre*%a%'y

Patients -ith N# -ho *ecome pregnant and take antiarrhythmic medications shold ha4e their

le4els measred *ecase they fre>ently re>ire adFstment. )n addition medication -ith

teratogenic effects eg amiodarone -hich is associated -ith fetal thyroid dysfnctionD shold *ereplaced if possi*le.

Patients -ith N# -ho *ecome pregnant and ha4e a pacemaker are ad4ised to perform fre>ent

pacemaker checks and make the appropriate adFstments especially -hen an increase in theleads threshold is notedD.

Patients -ith N# -ho *ecome pregnant and ha4e 4entriclar dysfnction de to

cardiomyopathy or a Mstard or ently sed in sdden

onset *radyarrhythmias. Althogh it may also *e sed for the initial treatment of chronic

arrhythmias cardiac pacing is preferred for longterm control.

2ie- fll drg information

A)r.&i%e

Atropine increases the heart rate throgh 4agolytic effects casing an increase in cardiac otpt.

&.$ mg P" >$(hr P8N

6eta'/6eta% Adrenergic Agonists

Cla++ Smmary

,hen gi4en systemically isoproterenol stimlates *eta receptors in the heart -hich prodces

positi4e inotropic and chronotropic effects. 1his reslts in increased cardiac otpt.

http://emedicine.medscape.com/article/159645-overviewhttp://emedicine.medscape.com/article/151066-overviewhttp://emedicine.medscape.com/article/151066-overviewhttp://reference.medscape.com/drug/atreza-atropine-po-342061http://reference.medscape.com/drug/atreza-atropine-po-342061http://emedicine.medscape.com/article/159645-overviewhttp://emedicine.medscape.com/article/151066-overviewhttp://reference.medscape.com/drug/atreza-atropine-po-342061http://reference.medscape.com/drug/atreza-atropine-po-342061


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D.+a*e F.rm+ > S)re%*)3+

Aam+-S).e+ A))a'+8 Caria' Arre+)8 .r Hear) :l.'

)2 *ols: &.&%&.&( mg '3 m? of a ':5&&&& diltionD initially 1HN doses of &.&'&.% mg

)2 infsion: 5 mcg/min '.%5 m? of a ':%5&&&& diltionD initially 1HN doses of %%&

mcg/min *ased on patients response

I+.&r.)ere%.l (I+&rel"

ICorticosteroids

Cla++ Smmary

1hese agents are sed to treat syncopal episodes cased *y flid or electrolyte im*alances. 1hey

restore flid and electrolyte *alance *y enhancing sodim rea*sorption in the kidney -hichreslts in epanded etracelllar flid 4olme. Mineralocorticoids also increase renal ecretion

of potassim and hydrogen ions.

)soproterenol has sympathomimetic effectsK specifically *eta' and *eta%adrenergic receptor agonist acti4ity.

Cardio4asclar "ther

Cla++ Smmary

1hese agents alter the P mechanisms responsi*le for arrhythmia. )n N# they may *e sed

-hen tachyarrhythmias occr. Patients mst *e careflly monitored to ascertain if

*radyarrhythmia is eacer*ated.


Di*.i% (La%.i%"

#igoin is a cardiac glycoside -ith direct inotropic effects as -ell as indirect effects on the

cardio4asclar system. )t acts directly on cardiac mscle increasing myocardial systoliccontractions. #igoins indirect actions reslt in increased carotid sins ner4e acti4ity and

enhanced sympathetic -ithdra-al for any gi4en increase in mean arterial pressre.


?i%ii%e

Einidine maintains normal heart rhythm follo-ing cardio4ersion of atrial fi*rillation or fltter.

)t depresses myocardial ecita*ility and condction 4elocity. Control the 4entriclar rate and

CH< if presentD -ith digoin or calcim channel *lockers *efore the administration of

>inidine.


Pr.&ra%.l.l (I%eral LA8 I%%.Pra% @L"

Propranolol is a class )) antiarrhythmic nonselecti4e *etaadrenergic receptor *lockerK it has

mem*ranesta*ili!ing acti4ity that decreases the atomaticity of contractions.

A)rial Firilla)i.%

http://reference.medscape.com/drug/isuprel-isoproterenol-342438http://reference.medscape.com/drug/lanoxin-digoxin-342432http://reference.medscape.com/drug/lanoxin-digoxin-342432http://reference.medscape.com/drug/quinaglute-quinidex-quinidine-342308http://reference.medscape.com/drug/quinaglute-quinidex-quinidine-342308http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364http://reference.medscape.com/drug/isuprel-isoproterenol-342438http://reference.medscape.com/drug/lanoxin-digoxin-342432http://reference.medscape.com/drug/lanoxin-digoxin-342432http://reference.medscape.com/drug/quinaglute-quinidex-quinidine-342308http://reference.medscape.com/drug/quinaglute-quinidex-quinidine-342308http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364http://reference.medscape.com/drug/inderal-inderal-la-propranolol-342364


22/23

Ra&i i*i)alii%* (l.ai%*-.+e" re*ime%

• )2: 7'% mcg/kg &.&&7&.&'% mg/kgD total loading doseK administer 5&G initiallyK then

may catiosly gi4e '/$ the loading dose >(7hr t-iceK perform carefl assessment of clinical

response and toicity *efore each dose

• P": '&'5 mcg/kg total loading doseK administer 5&G initiallyK then may catiosly gi4e

'/$ the loading dose >(7hr t-iceK peform carefl assessment of clinical response and toicity *efore each dose

Mai%)e%a%'e

• P": 3.$5.' mcg/kg/day or &.'%5&.5 mg/day P"K may increase dose e4ery % -eeks *ased

on clinical response serm drg le4els and toicity

• )2/)M: &.'&.$ mg >#ayK )M rote not preferred de to se4ere inFection site reaction

D.+a*e F.rm+ > S)re%*)3+

Arr3y)3mia+

?i%ii%e Sla)e

• 1est #ose: %&& mg P" >inidine slfate se4eral hr *efore fll dosage

• A%3hr ntil paroysm terminated

• Atrial/2entr Prematre Contractions: %&&3&& mg P" 1)#/E)#

• Maint: %&&$&& mg P" 1)#/E)# or (&& mg of 8 P" >7'%hr

• No more than 3$ g/d

?i%ii%e $l'.%a)e

• 3%$((& mg P" >7'%hr

• Maint: ($7 mg P" >'%hr "8 3%$((& mg P" >7hr • P21:$&& (&& mg P" >%3hr ntil paroysm is terminated

• )2: s 5 mg/kg *t may need p to '& mg/kgD at &.%5 mg/kg/min

pra4entriclar Arrhythmia

P": '&3& mg >(7hr

)2: '3 mg at ' mg/min initiallyK repeat >%5min to total of 5 mg

"nce response or maimm dose achie4ed do not gi4e additional dose for at least $ hors


23/23

sick sinus syndrome 1

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